title: Dynamic transcriptomes of human myeloid leukemia cells.
abstract: To identify the mechanisms controlling chronic myeloid leukemia (CML) and acute myeloid leukemia (AML) in humans, we analyzed genome-wide transcription dynamics in three myeloid leukemia cell lines (K562, HL-60, and THP1) using high-throughput sequencing technology. Using KEGG analysis, we found that the ERK/MAPK, JAK-STAT and ErbB pathways promoted proliferation and metabolism in CML. However, in AML, differentiation and apoptosis blocking resulted in the accumulation of blast cells in marrow. In addition, each cell type had unique characteristics. K562 cells are an ideal model for studying erythroid differentiation and globin gene expression. The chemokine signaling pathway and Fc gamma R-mediated phagocytosis were markedly upregulated in HL-60 cells. In THP1 cells, highly expressed genes ensured strong phagocytosis by monocytes. Further, we provide a new insight into myeloid development. The abundant data sets and well-defined analysis methods will provide a resource and strategy for further investigation of myeloid leukemia.
authors.affiliation: CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, No. 1-7 Beichen West Road, Chaoyang, Beijing 100101, China. Electronic address: wanghai@big.ac.cn.
authors.forename: Hai
authors.initials: H
authors.lastname: Wang
authors.forename: Haiyan
authors.initials: H
authors.lastname: Hu
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhang
authors.forename: Yadong
authors.initials: Y
authors.lastname: Yang
authors.forename: Yanming
authors.initials: Y
authors.lastname: Li
authors.forename: Yang
authors.initials: Y
authors.lastname: Hu
authors.forename: Xiuyan
authors.initials: X
authors.lastname: Ruan
authors.forename: Yaran
authors.initials: Y
authors.lastname: Yang
authors.forename: Zhaojun
authors.initials: Z
authors.lastname: Zhang
authors.forename: Chang
authors.initials: C
authors.lastname: Shu
authors.forename: Jiangwei
authors.initials: J
authors.lastname: Yan
authors.forename: Edward K
authors.initials: EK
authors.lastname: Wakeland
authors.forename: Quanzhen
authors.initials: Q
authors.lastname: Li
authors.forename: Songnian
authors.initials: S
authors.lastname: Hu
authors.forename: Xiangdong
authors.initials: X
authors.lastname: Fang
mesh_terms: D017209:Apoptosis / Q000235:genetics; D002454:Cell Differentiation / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D066246:ErbB Receptors / Q000502:physiology; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D018922:HL-60 Cells; D059014:High-Throughput Nucleotide Sequencing; D006801:Humans; D053612:Janus Kinases / Q000502:physiology; D020014:K562 Cells; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000378:metabolism*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000378:metabolism*; D020935:MAP Kinase Signaling System / Q000502:physiology; D053858:Metabolic Networks and Pathways / Q000235:genetics; D015398:Signal Transduction; D059467:Transcriptome
chemical_list: C512478:EGFR protein, human; D066246:ErbB Receptors; D053612:Janus Kinases
keywords: Acute myeloid leukemia; Chronic myeloid leukemia; High-throughput RNA sequencing